Abstract
Allergic rhinitis (AR) is an allergic disease characterized as (immunoglobulin, IgE)-mediated type I hypersensitivity disorder. Regulatory T cells (Tregs) play a crucial role in AR. In the present study, we aimed to investigate the mechanism of how Tregs are regulated by long noncoding RNA HCP5 and the regulatory role of HCP5 in IL-13-induced inflammatory response in nasal epithelial cells (NECs) from AR patients. Peripheral blood mononuclear cells (PBMCs) and NECs were obtained from collected blood samples and nasal epithelial tissues. CD4+ T cells and Tregs were purified using certain cell isolation kits from PBMCs and Tregs were also differentiated from CD4+ T cells using recombinant human IL-2 and TGF-β. The expression levels of HCP5, miR-16, ATXN2L, GM-CSF, eotaxin, and MUC5AC were detected by real-time PCR and western blot. The concentrations of inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). The interaction among HCP5, miR-16, and ATXN2L were verified by dual-luciferase reporter assay. lncRNA HCP5 expression dramatically downregulated in PBMCs, CD4+ T cells, Tregs, and nasal tissues of AR patients, as well as in IL-13-treated NECs. HCP5 promoted Tregs differentiation and proliferation via targeting miR-16/ATXN2L axis. Additionally, HCP5 inhibited IL-13-induced GM-CSF, eotaxin, and MUC5AC production in NECs. HCP5 sponged miR-16 and negatively regulated its expression, and miR-16 targeted ATXN2L and inhibition of miR-16 suppressed IL-13-induced GM-CSF, eotaxin, and MUC5AC expression. HCP5/miR-16/ATXN2L axis mediated Tregs proliferation and functions in AR. Besides, the regulation of IL-13-induced dysfunction of NECs by lncRNA HCP5 depended on miR-16/ATXN2L in the inflammatory response of AR.
Highlights
Allergic rhinitis (AR), the most common inflammatory disease of the nasal mucosa, is primarily mediated by serum immunoglobulin E (IgE) following contact with allergens and characterized by hypersecretion of mucus [1]
The long noncoding RNAs are defined as a group of single-stranded RNA with lengths longer than 200 bp that are not translated into protein [4]. lncRNAs reside in the nucleus or cytoplasm and interact with nucleic acids or proteins, and have been shown to regulate dosage compensation, genomic imprinting, pluripotency, cell differentiation and development, immune response, etc. lncRNAs bring about such copious functions by employing diverse mechanisms such as translational inhibition, mRNA degradation, RNA decoys, regulation of protein activity, and regulating the availability of miRNAs by sponging mechanism [5]
LncRNA Histocompatibility leukocyte antigen complex P5 (HCP5) Was Lowly Expressed in AR Patients
Summary
Allergic rhinitis (AR), the most common inflammatory disease of the nasal mucosa, is primarily mediated by serum immunoglobulin E (IgE) following contact with allergens and characterized by hypersecretion of mucus [1]. LncRNAs reside in the nucleus or cytoplasm and interact with nucleic acids or proteins, and have been shown to regulate dosage compensation, genomic imprinting, pluripotency, cell differentiation and development, immune response, etc. A lncRNA microarray analysis showed that a total of 2259 lncRNAs including 1033 up-regulated and 1226 down-regulated were significantly differentially expressed in the nasal mucosa samples from 4 AR patients as compared to those from 4 non-allergic subjects [7]. Their pathological effects on the development of allergic rhinitis (AR) have not been clearly understood
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